(Adapted from the Applicant's Abstract) The long-term objective of this project is to elucidate the role(s) of sickle red blood cells (SRBC) - endothelial cell (EC) - polymorphonuclear cell (PMN) interactions in sickle cell related acute lung injury The investigators further propose to investigate the potential role of PMN activation in initiating pulmonary microvascular occlusion by the SRBC. To achieve these objectives, the isolated-perfused rat lung model will be used with emphasis on the relationship of prolonged hypoxia with reoxygenation and ischemia (no flow, no ventilation) - reperfusion on initiating microvascular occlusion through mechanism which activate the intact vascular endothelium through the release of various cytokines such as IL-1, TNFalpha, and enhanced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1). In this proposal the investigators suggest the PMN is key in causing EC damage as associated with increased permeability edema and enhanced SRBC adhesogenicity to the vascular endothelium. SRBC adhesion/retention will be assessed using Cr51-labeled SRBC. Permeability edema will be used using the capillary filtration coefficient. Studies of the nature proposed will further the understanding in non-infectious causes of sickle acute lung injury.